Han T, Takita H
Cancer. 1980 Dec 1;46(11):2416-20. doi: 10.1002/1097-0142(19801201)46:11<2416::aid-cncr2820461120>3.0.co;2-g.
Indomethacin (prostaglandin synthetase inhibitor) was found to be capable of enhancing the mitogen-induced lymphocyte proliferative responses of healthy subjects and patients with lung cancer. A whole-blood culture technique was used. Indomethacin had no mitogenic activity. We observed a greater enhancement of lymphocyte response by indomethacin in weak responders as compared with strong responders in healthy subjects and lung cancer patients. A greater enhancement was also noted in lung cancer patients with active disease as compared with lung cancer patients in remission. In a separated cell culture system, the indomethacin exerted no effect on purified T cells in the absence of monocytes, while this agent exerted its enhancement effect on T lymphocyte response in the presence of autologous monocytes of lung cancer patients. This suggests that monocytes (suppressor cells) may secrete prostaglandins, which are responsible for the impairment of T lymphocyte response in lung cancer patients.
消炎痛(前列腺素合成酶抑制剂)被发现能够增强健康受试者和肺癌患者有丝分裂原诱导的淋巴细胞增殖反应。采用全血培养技术。消炎痛无促有丝分裂活性。我们观察到,与健康受试者和肺癌患者中的强反应者相比,消炎痛对弱反应者的淋巴细胞反应增强作用更大。与缓解期的肺癌患者相比,活动期肺癌患者的增强作用也更明显。在一个分离的细胞培养系统中,在没有单核细胞的情况下,消炎痛对纯化的T细胞没有作用,而在有肺癌患者自体单核细胞存在的情况下,该药物对T淋巴细胞反应发挥增强作用。这表明单核细胞(抑制细胞)可能分泌前列腺素,而前列腺素是导致肺癌患者T淋巴细胞反应受损的原因。